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Fast resupply of synaptic vesicles requires synaptotagmin-3
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Fast resupply of synaptic vesicles requires synaptotagmin-3
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Journal Article
Fast resupply of synaptic vesicles requires synaptotagmin-3
2022
Overview
Sustained neuronal activity demands a rapid resupply of synaptic vesicles to maintain reliable synaptic transmission. Such vesicle replenishment is accelerated by submicromolar presynaptic Ca
2+
signals by an as-yet unidentified high-affinity Ca
2+
sensor
1
,
2
. Here we identify synaptotagmin-3 (SYT3)
3
,
4
as that presynaptic high-affinity Ca
2+
sensor, which drives vesicle replenishment and short-term synaptic plasticity. Synapses in
Syt3
knockout mice exhibited enhanced short-term depression, and recovery from depression was slower and insensitive to presynaptic residual Ca
2+
. During sustained neuronal firing, SYT3 accelerated vesicle replenishment and increased the size of the readily releasable pool. SYT3 also mediated short-term facilitation under conditions of low release probability and promoted synaptic enhancement together with another high-affinity synaptotagmin, SYT7 (ref.
5
). Biophysical modelling predicted that SYT3 mediates both replenishment and facilitation by promoting the transition of loosely docked vesicles to tightly docked, primed states. Our results reveal a crucial role for presynaptic SYT3 in the maintenance of reliable high-frequency synaptic transmission. Moreover, multiple forms of short-term plasticity may converge on a mechanism of reversible, Ca
2+
-dependent vesicle docking.
Synaptotagmin-3 is identified as the presynaptic high-affinity calcium sensor to rapidly replenish synaptic vesicles to maintain steady synaptic transmission.
